Sudden death in patients with coronary artery disease is considered to be due to disturbances in heart rhythm (e.g. ventricular fibrillation or cardiac asystole). There are many signs that these arrhythmias occur because of hyperactivity in cardiac autonomic nerves. I propose to identify the parts of the nervous system that contribute to cardiac arrhythmias and define their contribution and the mechanism by which they operate to disrupt cardiac rhythm after coronary occlusion. These studies will be performed on cats and dogs and the techniques used to obtain this information are: (1) neural recordings from afferent and efferent cardiac nerves combined with measurements of indices of cardiac function (arterial blood pressure, EKG and cardiac contractility), (2) electrical stimulation of afferent nerves, central nervous system, and efferent nerves, and (3) denervation of afferent cardiac receptors. I plan to integrate the results into a comprehensive picture of the interaction of the heart and nervous system after coronary occulusion. I will also study the ability of drugs to modify each part of the system with the hope of finding those that can be used to benefit patients with coronary occlusions.